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| Status |
Public on Mar 10, 2021 |
| Title |
RNA-seq analysis of A549 cells harboring Smad3 R104K A105P mutation. |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Transforming growth factor-beta (TGF-beta) transmits signals that facilitate cancer progression. Especially, epithelial-mesenchymal transition (EMT) induced by TGF-beta is considered to crucially contribute to the malignant phenotype of cancer cells. Here we report that the EMT-associated cellular responses induced by TGF-beta are mediated through distinct signaling pathways that diverge at Smad3; cell motility and epithelial marker downregulation are Smad3-dependent while mesenchymal marker induction is not. Furthermore, using a chimeric protein approach in SMAD3 knockout A549 cells, we found that the beta 4 region in the MH1 domain of Smad3 is indispensable for TGF-beta–induced cell motility, but not for epithelial marker downregulation. A transcriptome analysis was performed using A549 cells expressing Smad3 mutant of the MH1 domain.
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| Overall design |
RNA-seq analyses were performed in wild type- and mutant Smad3 (R104K A105P)-expressing A549 lung adenocarcinoma cells stimulated with TGF-beta.
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| Contributor(s) |
Motizuki M, Koinuma D, Yokoyama T, Itoh Y, Omata C, Miyazono K, Saitoh M, Miyazawa K |
| Citation(s) |
33741342 |
| Submission date |
Jun 08, 2020 |
| Last update date |
May 06, 2021 |
| Contact name |
Daizo Koinuma |
| E-mail(s) |
d-koinuma@umin.ac.jp
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| Organization name |
University of Tokyo
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| Department |
Pathology
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| Street address |
Hongo 7-3-1, Bunkyo-ku
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| City |
Tokyo |
| ZIP/Postal code |
113-0033 |
| Country |
Japan |
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| Platforms (1) |
| GPL17303 |
Ion Torrent Proton (Homo sapiens) |
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| Samples (8)
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| Relations |
| BioProject |
PRJNA638101 |
| SRA |
SRP266451 |
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